Hydrogen sulfide protects against apoptosis under oxidative stress through SIRT1 pathway in H9c2 cardiomyocytes

Wu, Dan; Hu, Qingmin; Liu, Xinhua; Pan, Li-Long; Xiong, Qinghui; Zhu, Yi‐Zhun

doi:10.1016/j.niox.2014.11.006

Cited by 85 publications

(78 citation statements)

References 42 publications

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“…We found that NOS inhibition completely reversed the protective effects of Na 2 S and partially those of thiovaline in vitro. In line with this finding, Wu et al (2015) showed that H 2 O 2 cytotoxicity was associated with decreased expression and phosphorylation (S1176) of eNOS and that treatment with another sulfide salt (NaHS) increased the ratio of p-eNOS/ eNOS. In sharp contrast, to Na 2 S and thiovaline, the protective effect of GYY4137 and AP39 remained unaffected by L-NAME, suggesting that these agents exerted NO-independent effects.…”

Section: Discussionsupporting

confidence: 60%

“…H 2 S donors, including diallyl disulfide and S-propargylcysteine, have been shown to rescue cultured cardiomyocytes from high glycose injury, doxorubicin-induced toxicity or ROStriggered injury (Szabó et al, 2011;Guo et al, 2013;Wu et al, 2015;Yang et al, 2015). The mechanisms through which H 2 S donors have been proposed to exerts their protective effects in these cultured cell systems include ATP-sensitive potassium channel and Akt activation, inhibition of mitogen-activated protein kinases pathways (p38, c-Jun N-terminal protein kinases), and inhibition of endoplasmic reticulum stress, as well as antioxidant mechanisms (Szabó et al, 2011;Wang, 2012;Guo et al, 2013;Salloum, 2015;Wu et al, 2015;Yang Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms through which H 2 S donors have been proposed to exerts their protective effects in these cultured cell systems include ATP-sensitive potassium channel and Akt activation, inhibition of mitogen-activated protein kinases pathways (p38, c-Jun N-terminal protein kinases), and inhibition of endoplasmic reticulum stress, as well as antioxidant mechanisms (Szabó et al, 2011;Wang, 2012;Guo et al, 2013;Salloum, 2015;Wu et al, 2015;Yang Fig. 6.…”

Section: Discussionmentioning

confidence: 99%

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Cardioprotection by H2S Donors: Nitric Oxide-Dependent and -Independent Mechanisms

Chatzianastasiou

Bibli²,

Andreadou³

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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Hydrogen sulfide (H 2 S) is a signaling molecule with protective effects in the cardiovascular system. To harness the therapeutic potential of H 2 S, a number of donors have been developed. The present study compares the cardioprotective actions of representative H 2 S donors from different classes and studies their mechanisms of action in myocardial injury in vitro and in vivo. Exposure of cardiomyocytes to H 2 O 2 led to significant cytotoxicity, which was inhibited by sodium sulfide (Na 2 S), thiovaline (TV), GYY4137[morpholin-4-ium 4 methoxyphenyl(morpholino) phosphinodithioate], and AP39 [(10-oxo-10-(4-(3-thioxo-3H-1,2-dithiol5yl)-phenoxy)decyl) triphenylphospho-nium bromide]. Inhibition of nitric oxide (NO) synthesis prevented the cytoprotective effects of Na 2 S and TV, but not GYY4137 and AP39, against H 2 O 2 -induced cardiomyocyte injury. Mice subjected to left anterior descending coronary ligation were protected from ischemia-reperfusion injury by the H 2 S donors tested. Inhibition of nitric oxide synthase (NOS) in vivo blocked only the beneficial effect of Na 2 S. Moreover, Na 2 S, but not AP39, administration enhanced the phosphorylation of endothelial NOS and vasodilator-associated phosphoprotein. Both Na 2 S and AP39 reduced infarct size in mice lacking cyclophilin-D (CypD), a modulator of the mitochondrial permeability transition pore (PTP). Nevertheless, only AP39 displayed a direct effect on mitochondria by increasing the mitochondrial Ca 21 retention capacity, which is evidence of decreased propensity to undergo permeability transition. We conclude that although all the H 2 S donors we tested limited infarct size, the pathways involved were not conserved. Na 2 S had no direct effects on PTP opening, and its action was nitric oxide dependent. In contrast, the cardioprotection exhibited by AP39 could result from a direct inhibitory effect on PTP acting at a site different than CypD.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cardioprotection by H2S Donors: Nitric Oxide-Dependent and -Independent Mechanisms

Chatzianastasiou

Bibli²,

Andreadou³

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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“…Two other studies showed protective effects of H 2 S containing water [88] and a mitochondrially-targeted H 2 S donor (AP39) [89] against oxidative stress and oxidative DNA damage in peripheral blood mononuclear cells of Alzheimer's patients and a murine brain microvascular endothelial cell line, respectively, again showing the positive effects of increased intracellular H 2 S on nuclear and mitochondrial genome stability. These and other studies also described improved cell viability [88, 90] and affected mitochondrial activity [89] after H 2 S administration.…”

Section: Hydrogen Sulfide and Agingmentioning

confidence: 52%

The role of hydrogen sulfide in aging and age-related pathologies

Perridon

Leuvenink

Hillebrands

et al. 2016

Aging

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When humans grow older, they experience inevitable and progressive loss of physiological function, ultimately leading to death. Research on aging largely focuses on the identification of mechanisms involved in the aging process. Several proposed aging theories were recently combined as the ‘hallmarks of aging’. These hallmarks describe (patho-)physiological processes that together, when disrupted, determine the aging phenotype. Sustaining evidence shows a potential role for hydrogen sulfide (H2S) in the regulation of aging.Nowadays, H2S is acknowledged as an endogenously produced signaling molecule with various (patho-) physiological effects. H2S is involved in several diseases including pathologies related to aging. In this review, the known, assumed and hypothetical effects of hydrogen sulfide on the aging process will be discussed by reviewing its actions on the hallmarks of aging and on several age-related pathologies.

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“…For example, H 2 S upregulated SIRT1 to inhibit endoplasmic reticulum stress in PC12 cells [67] and to prevent H 2 O 2 -induced [68] or nicotinamide-induced [69] senescence in human umbilical vein endothelial cells (HUVECs). Besides HUVECs, previous studies from our group demonstrated that H 2 S increased SIRT1 expression to abolish the oxidative stress induced apoptosis in H9c2 cardiomyocytes [70] and previous studies from our group demonstrated [6] found that H 2 S attenuated inflammatory hepcidin partially by promoting SIRT1-mediated STAT3 deacetylation. SIRT3, one of the isoforms of SIRT family, has also been reported that it could be regulated by H 2 S to protect endothelial cells in an antioxidant manner [71].…”

Section: H2s Epigenetic Regulation Atherosclerosis Is An Important Famentioning

confidence: 83%

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

Zj¹,

Wu²,

Guo³

et al. 2017

Cell Physiol Biochem

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Hydrogen sulfide (H₂S) is now admitted as a third gasotransmitter together with nitric oxide (NO) and carbon monoxide (CO), albeit it was originally considered as a foul and poisonous gas. Endogenous H₂S production in mammalian cells is counting on the three enzymes acting on cysteine. Involvement of H₂S in various physiological and pathological processes has been extensively studied in the last fifteen years. Mounting evidence suggests that H₂S is able to protect against atherosclerosis development and progression. Exogenous H₂S supplement has salutary effects on atherogenesis, and reduction of the endogenous H₂S level accelerates atherosclerosis. The anti-atherosclerotic mechanisms of H₂S have been descried in different aspects, including endothelium preservation, antioxidative action, anti-inflammatory responses, vasorelaxation, regulation of ion channels, etc. However, further investigation is still needed to help us gain more insights into the fundamental underlying mechanisms, and that will allow us to design better therapeutic applications of H₂S in the treatment of atherosclerosis.

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Hydrogen sulfide protects against apoptosis under oxidative stress through SIRT1 pathway in H9c2 cardiomyocytes

Cited by 85 publications

References 42 publications

Cardioprotection by H2S Donors: Nitric Oxide-Dependent and -Independent Mechanisms

Cardioprotection by H2S Donors: Nitric Oxide-Dependent and -Independent Mechanisms

The role of hydrogen sulfide in aging and age-related pathologies

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

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